Background The hypotension of septic shock is due to systemic vasodila
tion. On the basis of a clinical observation, we investigated the poss
ibility that a deficiency in vasopressin contributes to the vasodilati
on of septic shock. Methods and Results In 19 patients with vasodilato
ry septic shock (systolic arterial pressure [SAP] of 92+/-2 mm HE [mea
n+/-SE], cardiac output [GO] of 6.8+/-0.7 L/min) who were receiving ca
techolamines, plasma vasopressin averaged 3.1+/-1.0 pg/mL. In 12 patie
nts with cardiogenic shock (SAP, 99+/-7 mm Hg; CO, 3.5+/-0.9 L/min) wh
o were also receiving catecholamines, it averaged 22.7+/-2.2 pg/mL (P<
.001). A constant infusion of exogenous vasopressin to 2 patients with
septic shock resulted in the expected plasma concentration, indicatin
g that catabolism of vasopressin is not increased in this condition. A
lthough vasopressin is a weak presser in normal subjects, its administ
ration al 0.04 U/min to 10 patients with septic shock who were receivi
ng catecholamines increased arterial pressure (systolic/diastolic) fro
m 92/52 to 146/66 mm Hg (P<.001/P<.05) due to peripheral vasoconstrict
ion (systemic vascular resistance increased from 644 to 1187 dyne . s/
cm(5); P<.001). Furthermore, in 6 patients with septic shock who were
receiving vasopressin as the sole presser, vasopressin withdrawal resu
lted in hypotension (SAP, 83+/-3 mm Hg), and vasopressin administratio
n at 0.01 U/min, which resulted in a plasma concentration (approximate
to 30 pg/mL) expected for the level of hypotension, increased SAP fro
m 83 to 115 mm Hg (P<.01). Conclusions Vasopressin plasma levels are i
nappropriately low in vasodilatory shock, most likely because of impai
red baroreflex-mediated secretion. The deficiency in vasopressin contr
ibutes to the hypotension of vasodilatory septic shock.